Neurovascular Coupling: Novel Insights from Studies in Awake Head-Fixed and Anesthetized Mice скачать в хорошем качестве

Neurovascular Coupling: Novel Insights from Studies in Awake Head-Fixed and Anesthetized Mice

Join Dr. Barbara Lind and Dr. Adrián Rodríguez-Contreras as they discuss neurovascular coupling in awake head-fixed and anesthetized mice, with a focus on the effects of anesthetics. Neurovascular coupling (NVC) modulates cerebral blood flow to match increased metabolic demand during neuronal excitation. While we know that astrocyte calcium levels rise with excitatory neurotransmission, much less is understood about astrocytic sensitivity to inhibitory neurotransmission. In addition, general anesthetics, widely used in both clinical practice and preclinical research, have been shown to cause large disruptions in cerebral blood flow, brain metabolism, NVC, and functional connectivity. This suggests that they may have direct and indirect effects on the physiology of cerebrovascular endothelial cells (CEC). In this webinar, Dr. Barbara Lind (Assistant Professor at the University of Copenhagen) and Dr. Adrián Rodríguez-Contreras (Associate Professor at Northwestern University) try to fill some of our knowledge gaps concerning NVC. Their insights stem from recent two-photon imaging and optogenetics studies performed in awake head-fixed and anesthetized mice. The presentations will elucidate the roles of astrocytes, interneurons, CECs, and calcium signaling in vivo, and specifically the effects of anesthesia on NVC. Key Topics Include: Advantages, limitations, and important considerations for using optical methods to investigate neurovascular physiology in animal models The effects of general anesthetics on cerebrovascular functions, including the diversity in astrocytic calcium responses to interneuronal activation Advantages of studying NVC in awake head-fixed mice and the available solutions Hypotheses that explain cerebrovascular responses to experimental manipulations Astrocytic responses to parvalbumin interneuron activation and their contribution to GABA-mediated NVC